Cardiac Surgery Core 3.17.16.

Cardiac Surgery Core

Anatomy Arterial supply Coronary arteries arise from?
Sinuses of Valsalva Origin of the left and right coronary arteries? Left= posteromedial Right= anteriomedial

Arterial supply Branches of left coronary artery?
Left anterior descending and left circumflex arteries Branches of LAD and respective area of supply? Diagonal branches- anterolateral LV wall Septal perforators- interventricular wall LAD overall supplies >50% LV mass and most of IV septum- most important surgical vessel Extends up to apex, where anastomoses with PDA

Arterial supply Course and supply of circumflex?
Runs along left AV groove Gives off obtuse marginal branches Terminates as left posterolateral branch What is the ramus intermedius? Dominant epicardial vessel that arises from trifurcation of LCA Landmark? Left atrial appendage

Arterial supply Branches of right coronary artery? Supply of AV node?
Multiple right ventricular branches (aka acute marginal branches) Posterior descending artery (80-85%) Right posterolateral artery Bifurcates over posterior IV sulcus Supply of AV node? RCA 90% Supply of SA node? 50% RCA, 50% LCA

Arterial supply

Venous drainage 3 principal systems?
Coronary sinus and its tributaries Receives 85% coronary venous blood Predominantly drains LV Lies within posterior AV groove, drains into RA Thebesian veins Small venous tributaries Drain directly into chambers Anterior cardiac veins Drains right coronary system Enters directly into RA or joins coronary sinus just proximal to orifice

Valvular anatomy Mitral valve
2 leaflets- anterior (aortic) and posterior (mural) 2 papillary muscles- posterior and anterior, both arise from LV wall Chordae tendinae connect leaflets and papillary muscles

Mitral valve Anterior leaflet Anterior base, ⅓ annulus circumference
Extends to aortic annulus Posterior leaflet Attached to ⅔ circumference of annulus Separated by 2 distinct commissures

Mitral valve Key surgical landmarks?
Circumflex artery runs over posterior mitral annulus Aortic valve (noncoronary leaflet) closely located to and contiguous with anterior leaflet AV node located deep to posteromedial commissure

Aortic valve 3 thin leaflets Surgical landmarks?
Attached in 3 sinuses of Valsalva Right coronary, left coronary, and noncoronary leaflets Surgical landmarks? Commissure between left and noncoronary leaflets located over MV anterior leaflet Commissure between right and noncoronary leaflets located over left bundle of His

Other valves Tricuspid valve Pulmonary valve
3 leaflets- large anterior, posterior, and septal Pulmonary valve Like aortic valve, consists of 3 cusps What is the nodulus of Arantius? Thickening formed by junction of lunulae/ cusps Coaptation of 3 cusps allow for seal

Physiology Driving force in myocardial perfusion?
Aortic pressure! Response to increased myocardial O2 demand? Increased coronary blood flow- up to 4-7x Resting near maximal O2 extraction Regulatory factors for increased blood flow? Adenosine NO CO2, O2 tension, H and K ions... adenosine- vascular SM relaxation resulting in vasomotor relaxation, coronary vasodilation, and increased blood flow NO- produced by endothelium, cause vasodilation too

Physiology Blood flow to heart occurs during? In exercise?
Diastole (approx 60%) In systole, increased intracavitary pressures exceed intracoronary pressure, thus impeding coronary blood flow! In exercise? Increased HR reduces diastolic time but compensates by vasodilation

Electrophysiology Location of SA node? Location of AV node?
Junction of SVC and RA Blood supply? 50% RCA, 50% LCA Per anatomist, way to define “dominance” Location of AV node? Interatrial septum, near coronary sinus orifice

Electrophysiology? From SA to AV node?
Impulse propagated to bundle of His, down membranous IV septum just below tricuspid valve Separates into left and right branches as progress into muscular IV septum

Cardiac mechanics Five main factors? Starling’s law? Rate Rhythm
Preload aka end-diastolic ventricular volume Afterload aka aortic pressure gradient Contractility Starling’s law? Relationship between EDV and contractility

Cardiac cycle

Coronary Artery Disease
Risks factors? Smoking, HTN, HLD, DM, male gender, obesity, older age, rheumatoid arthritis, +FH Pathophysiology key= endothelial injury Foam cells and “fatty streak” SM proliferation, resulting in wall injury Formation of fibrous cap/plaque in response to intimal disruption and collagen exposure Angiogenesis Plaque rupture and resulting thrombosis Concerning signs for plaque rupture= large eccentric soft lipid core, thin fibrous cap, inflammation w/in cap and adventitia, increased plaque neovascularity, and evidence of outward or positive vessel remodeling

CAD Usually involves stenosis of proximal coronary arteries or near junctions Common presentations Angina- due to reversible myocardial ischemia without cellular necrosis Usually precipitated by exertion (increased myocardial O2 demand) and resolves with rest and/or nitrates Unstable angina- resting or accelerated May be absent in approx 15% CAD patients

CAD presentations Acute MI
Reflects irreversible myocardial injury and cell death If 40% or more of ventricular mass involved, will result in cardiogenic shock and usually death Signs and symptoms? SOB, retrosternal chest pain, diaphoresis, N/V EKG changes Elevated troponin levels

Sequelae of acute MI Arrhythmias (within 1st 24hrs)
CHF- usually if 25% or more LV myocardium infarcted Interventricular septal rupture (2%) Usually 3-5 days but up to 2 wks post MI 60% anterior wall, 40% inferior wall Dx: step-up O2 content from RA and pulmonary artery >9%, echocardiogram 75% patients survive and need surgical repair New York Heart Association Classification

NY Heart Assoc Classification

Sequelae of acute MI Free wall rupture
Leads to hemopericardium and cardiac tamponade Usually fatal Papillary muscle rupture/ dysfunction Associated with MI of posteroinferior wall Leads to acute MR Ultimately needs operative repair Ventricular aneurysm (5-10%) Majority anteroseptal aspect of LV with MI in LAD distribution Complications- CHF, decreased EF, ischemic re-entrant ventricular arrhythmias, and shower emobli

Sequelae of acute MI Chronic ischemic cardiomyopathy
Develops after multiple MI’s Most common in small vessel disease (diabetics)

Treatment of CAD First line- lifestyle modifications and medical management PTCA Contraindications- LCA dz, 3 vessel dz, or complex obstructive lesions Risks of re-stenosis 20-30% within 1st year Drug-eluting stents inhibit neointimal hyperplasia and may decrease re-stenosis but no change in overall mortality

Question Indications for CABG surgery include all of the following except: Severe triple-vessel occlusive disease Stenosis of left main coronary artery Persistent angina and ECG changes following PCI Acute MI Development of complications during PTCA

Question After a documented acute MI, surgery is indicated in all but which of the following situations? Postinfarction angina with anatomic lesions not amenable to PTCA VSDs Acute MR Free wall rupture Atrial tachyarrhythmia

Coronary Artery Bypass Graft
Indications? Angina refractory to medical mgmt Unstable angina CHF with large area of viable myocardium STEMI with failed PTCA and/or cardiogenic shock Left main disease (>50%) Left main equivalent dz (LAD>70% stenosis and proximal left complications) 3 vessel disease 2 vessel disease with proximal LAD stenosis and LVEF <50% or extensive ischemia on imaging Life-threatening post MI complications

CABG Preoperative work-up
Carotid duplex and/or imaging- a/w LCA stenosis CXR, PFT’s Peripheral vascular evaluation Rule out subclavian stenosis- precludes use of internal mammary conduit ECG, echocardiogram Thallium imaging Coronary arteriography CT angiography- high NPV, low PPV

Basic steps of CABG Median sternotomy
Heparinization and CPB cannulation and establishment Myocardial arrest Distal anastomosis(es) Restoration of electromechanical activity Proximal anastomosis(es) CPB wean Surgical drainage and closure

CABG Conduit choices? Left internal thoracic artery- patency 98% at 5 years, 95% at 10 yrs, and 88% at 15 yrs Right ITA- 96% at 5yrs, 81% at 10yrs, and 65% at 15 yrs Saphenous veins- 80% 10 yrs to LAD, 50% to circumflex or RCA Radial artery- 96% at 1 yr, 89% 4 yrs, 83% 10 yrs

Question Which of the following is the maximum time that extracorporeal circulation can be tolerated before significant risk for physiologic injury and metabolic defects occur? 2-4 hours 6-8 hours 10-12 hours 14-16 hours 18-20 hours B COMMENTS: Tolerance of extracorporeal circulation (CPB) is variable. Six to 8 hours is an acceptable range, although physiologic injury may occur earlier. Occasionally, patients undergo longer perfusion with relatively few consequences. With proper myocardial preservation, the heart can be arrested safely for up to 4 hours. Physiologic defects observed with extracorporeal circulation include progressive sludging of blood elements in the capillary microcirculation, red blood cell hemolysis, coagulation defects, denaturation of plasma proteins, fibrinolysis, and activation of inflammatory cascades. The primary culprit within the CPB circuit for these derangements is the oxygenator and its vast surface area for blood–foreign body exposure.

Cardiopulmonary Bypass
CPB- 1st introduced in 1954 by Dr. Gibbon Requires heparinization Venous reservoir- stores blood volume Membrane oxygenator- gas exchange Heat exchanger Arterial pump Cannulae and pump tubing Left atrial vent Hyperkalemic perfusate- causes cardiac arrest in diastole

CPB Physiological effects of prolonged CPB?
Sludging of blood in capillaries Hemolysis Coagulation defects Denaturation of plasma proteins Fibrinolysis Activation of inflammatory cascades Related to blood-foreign body exposure from oxygenator

CPB Physiologic thresholds to meet before weaning CPB?
Resumption rhythmic electromechanical activity Temperature >36.5 Adequate reserve blood volume Normal systemic K levels Resumption of ventilation with adequate ABG’s

Question Angina develops in a patient 5 years after CABG surgery. Angiography most likely reveals which of the following? Vein graft thrombosis Progressive atherosclerosis in the vein graft Progressive atherosclerosis in the coronary arteries A dominant right coronary system Occlusion of the left internal mammary arterial graft C COMMENTS: The rate of recurrence of angina following CABG surgery is approximately 5% to 7% per year. Surgery, unfortunately, does not slow the progression of atherosclerosis, which is the primary cause of recurrent symptoms. Graft occlusion may also occur as a result of thrombosis, intimal fibrosis, or fibrous endarteritis. Vein grafts may also be involved with atherosclerosis, which usually occurs later during the postoperative course. Overall, the rate of vein graft patency is approximately 70% to 80% after 5 years. Internal mammary artery grafts have significantly higher long-term patency and improved event-free survival rates in com- parison with vein grafts

CABG statistics More than 90% patients have initial relief of angina symptoms Periop mortality rates range from 1-2% in low risk pts to 10-15% in high risk patients

Postop considerations
Aggressive normothermia maintenance Minimum cardiac index 2L/min/m2 and ScvO2 >60% Arrhythmias % post-cardiac surgery patients, esp if received inotropic meds Postop afib approx 30%, peak POD2 Postperfusion syndrome RF’s- length of CPB>4hrs, older age

Other postop considerations
Cardiac tamponade Characteristic Swan-Ganz parameters? Other signs and symptoms? Perioperative MI (1-2%) Postop hemorrhage- re-exploration needs in up to 5% pts Avoid clots in mediastinal and chest tubes- can result in cardiac tamponade

Question Following open heart surgery, a patient experiences chest pain, fever, tachycardia, and a pericardial friction rub. Which of the following statements is true? The most likely diagnosis is postop mediastinitis. Primary treatment should include surgical exploration. The patient most likely responds well to antibiotics. There is usually an associated leukocytosis or lymphocytosis. This syndrome is usually accompanied by pleural effusion and shortness of breath.

Postop complications Postpericardiotomy aka Dressler syndrome
Transient delayed pericardial inflammatory reaction, 2-4 wks postop usually Ssx’s: fever, anterior chest pain, pericardial friction rub, pleuritis Dx: elevated WBC and lymphocytes, elevated ESR May lead to mediastinal fibrosis and premature graft occlusion Tx: NSAIDs for 2-4 wks, steroids for refractory cases

Questions The physiologic effects of the intra-aortic balloon pump include which of the following? Decreased cardiac afterload Decreased coronary blood flow Increased left ventricular end-diastolic pressure Decreased cerebral perfusion Increased left ventricular preload A COMMENTS: Indications for use of the intra-aortic balloon pump include the following: cardiac failure after CPB, refractory unstable angina, preoperative treatment of septal defects, mitral regurgitation, arrhythmias, ventricular aneurysms, and occasionally, cardiogenic shock. The IABP is used to treat cardiogenic shock associated with myocardial infarction, but only 15% to 20% of patients can be weaned successfully from this device, and there is no conclusive evidence that an IABP decreases infarct size. The IABP is particularly effective in controlling pain in patients with angina refractory to pharmacologic manipulation. The device has also been successful in the support of patients with cardiac failure following CPB. Most such patients can be weaned successfully, with excellent long-term survival. Severe aortic insufficiency is a contraindication to use of the IABP because regurgitation and cardiac failure are exacerbated with its use.

Questions Which of the following statements describes the clinical effects of the intra-aortic balloon pump (IABP)? Use of an IABP in patients with MI and cardiogenic shock decreases infarct size. Most patients using an IABP for cardiogenic shock after MI can be weaned from this device. An IABP effectively relieves pain in pts with unstable angina. An IABP is not indicated for support of cardiac failure following CBP because of availability of VADs. An IABP is indicated in patients with severe aortic insufficiency to decrease peripheral resistance C COMMENTS: Indications for use of the intra-aortic balloon pump include the following: cardiac failure after CPB, refractory unstable angina, preoperative treatment of septal defects, mitral regurgitation, arrhythmias, ventricular aneurysms, and occasionally, cardiogenic shock. The IABP is used to treat cardiogenic shock associated with myocardial infarction, but only 15% to 20% of patients can be weaned successfully from this device, and there is no conclusive evidence that an IABP decreases infarct size. The IABP is particularly effective in controlling pain in patients with angina refractory to pharmacologic manipulation. The device has also been successful in the support of patients with cardiac failure following CPB. Most such patients can be weaned successfully, with excellent long-term survival. Severe aortic insufficiency is a contraindication to use of the IABP because regurgitation and cardiac failure are exacerbated with its use.

Intra-aortic balloon pump
Indications? Circulatory support in patients with profound myocardial dysfunction Low cardiac output states, cardiogenic shock Unstable angina refractory to medical therapy Post-MI reversible cardiac defects (ex. acute MR) Post-op CPB wean

IABP Principal effects? Reduce afterload Improve LVEF
Reduce myocardial O2 consumption Increase diastolic coronary blood flow (increases diastolic BP)

IABP Inserted via femoral artery usually
Positioned just distal to left subclavian artery Mechanism of action in relation to cardiac cycle? Inflates during diastole (corresponds to T wave peak/middle) Deflates during systole (corresponds to R wave peak)

IABP complications Femoral artery injury Aortic perforation
LE ischemia Reduced flow to kidneys and other organs Balloon rupture

Valvular disease

Question Aortic stenosis in an adult may result from all of the following except: Ehlers-Danlos syndrome Marfan syndrome Rheumatic fever Syphillis Bacterial endocarditis C

Question Clinical manifestations of severe aortic stenosis include all of the following except: Syncope Holosystolic murmur Angina pectoris Dyspnea on exertion Atrial fibrillation

Aortic stenosis #1 cause- senile degeneration and calcification of bicuspid or less often normal valve Usually asymptomatic until late in course Progressive LV hypertrophy resulting in decreased LV compliance and eventually decreased cardiac output Symptomatic once valve area 1cm2 or less

Aortic stenosis Signs:
Mid-systolic ejection murmur radiating to neck and decreased by standing/sitting Diminished carotid pulses Forceful sustained nondisplaced apical impulse Symptoms: Angina (65%)- mean 5 yr survival Syncope (15-25%)- mean 3 yr survival CHF- worst prognostic factor, mean survival 2 years

Question Indications for surgery in patients with aortic stenosis include all of the following except: All symptomatic patients Systolic pressure gradient >50mmHg in asymptomatic patients Associated pericardial effusion Valvular cross-section area smaller than 1cm2 Serial radiographic evidence of rapid cardiac enlargement C

Aortic stenosis Indications for operative replacement:
Severe AS- valve area <0.75-1cm 2, mean gradient >40-50mmHg, or jet velocity >4m/sec Asymptomatic patients undergoing CABG or other cardiac surgery Severe AS and LV systolic dysfunction (EF<0.5)

Aortic insufficiency Causes? Myxomatous degeneration
Rheumatic heart disease Endocarditis Syphillis Connective tissue d/o’s Inflammatory dz HTN Aortic dissection

AI continued Chronic AI- manifests as symmetric wall thickening and ventricular enlargement due to volume overload Signs? Decrescendo diastolic murmur Corrigan’s water-hammer pulse- hyperdynamic circulation with markedly inc pulse pressure Forcefully and laterally displaced apical pulse Symptoms? Dyspnea on exertion, weakness...

AI Acute aortic insufficiency Lack of compensatory chamber enlargement
Presents with fulminant pulm edema, myocardial ischemia, and CV collapse

Question Indications for the operative intervention to correct aortic insufficiency include which of the following? Finding of AI alone, which warrants correction even in asymptomatic patients Loudness and length of diastolic murmur LVEDV 40ml/m2 Magnitude of regurgitation Age of patient D

AI Indications for surgery: Severe aortic insufficiency
Chronic moderate to severe AI with LV dysfunction (LVEF<0.5) Chronic AI undergoing other cardiac surgery Functional class II heart failure

Transcatheter AV interventions
Alternative to conventional operative AVR Implanted via transfemoral or transapical approach Avoid CPB Associated with estimated 20% reduction of mortality at 1yr in high risk pts

Question 3 hours after AVR, a patient suddenly becomes hypotensive. Cardiac index has decreased from 2.5 to 1.6L/min. CVP is 19mmHg and PCWP is 20mmHg. Mediastinal drainage over the last hr has been minimal. Immediate treatment includes which of the follow? Echocardiogram to assess prosthetic valve function Volume resuscitation to increase cardiac output Afterload reduction with nitroprusside Preload reduction with nitroglycerin Mediastinal exploration Equalization of diastolic pressures s/o cardiac tamponade!

Question What is the most common cause of mitral insufficiency in Western countries? Bacterial endocarditis Degenerative mitral valve disease Marfan syndrome Silent MI Rupture of chordae tendineae B

Mitral stenosis Causes:
Rheumatic fever #1 Collagen vascular disease, amyloidosis… Left atrial pressure overload leading to left atrial dilatation Ventricles spared LV dilatation >45mm associated with high incidence of atrial fibrillation and thus TE events Transvalvular gradient present when valve area <2cm2 “Critical” MS= valve area <1cm2

Mitral stenosis Signs: apical “rumbling” mid-diastolic murmur, opening snap, loud S1 Symptoms- develop late in course Dyspnea (due to pulm congestion), dec LV preload, afib Can develop mural thrombi- 50% to cerebral circulation

Question Indications for valve replacement in patients with significant mitral stenosis include all of the following except: CHF Pulmonary hypertension Atrial fibrillation Asymptomatic state Systemic embolization

Question With regards to the results of surgical treatment of symptomatic MS, which of the following statements if false? Survival rate is higher than after medical tx Commissurotomy decreases the risk for systemic embolization and endocarditis. Pulmonary vascular resistance usually diminishes folowing valve replacement or commissurotomy 10-yr survival exceeds 90% Recurrent valvular dysfunction is best treated by mitral valve repair E

Question With regards to the results of surgical treatment of symptomatic MS, which of the following statements if false? Survival rate is higher than after medical tx Commissurotomy decreases the risk for systemic embolization and endocarditis. Pulmonary vascular resistance usually diminishes following valve replacement or commissurotomy 10-yr survival exceeds 90% Recurrent valvular dysfunction is best treated by mitral valve repair E

MS continued Indications for surgery: Moderate to severe MS
Pressure gradient >25mmHg or valve area less than 1.5cm2 Asymptomatic patients with severe pulm HTN

Mitral regurgitation #1 cause myxomatous degeneration
Other causes- endocarditis, MI, ischemic papillary muscle rupture/dysfunction, rheumatic disease Results in LV and LA pressure overload, causing increased wall tension, chamber enlargement and wall thickening (symmetric) Eventually leads to worsening LA compliance, pulm congestion, and right heart failure

MR Indications for surgery: Symptomatic pts with NYHA class II-IV
Asymptomatic pts with chronic severe MR and mild-to-moderate LV dysfunction (EF<0.6) Asymptomatic pts with chronic severe MR and new onset afib or pulm HTN\ Repair favored over MV replacement

Question With regards to patients with MR versus those with MS, which of the following statements is true? LV failure is more common. Atrial fibrillation rarely occurs. Systemic emboli are frequent. The postop prognosis is better following replacement than repair. Pulmonary hypertension usually fails to resolve following valve replacement A

Valve types Bioprostheses: Mechanical valves: Low TE rate
Less durable- faster deterioration with younger patients compared to elderly (?60) Overall 10-15yr mean to failure Mechanical valves: Excellent durability Higher risks for TE event (0.5-3% per year) Requires lifelong anticoagulation

Question With respect to the selection of prosthetic heart valves, all of the following are true except: Free aortic homograft valves have a lower incidence of infective endocarditis than porcine valves. Bioprosthetic valves should be avoid in patients with chronic renal failure Mechanical valves should be avoided in children Current bioprosthetic valves are less durable than mechanical valves. Reconstructed mitral valves have limited durability and offer no advantage to valve replacement E

Questions?

Cardiac Surgery Core 3.17.16.

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